Shear and Pressure-Induced Mechanotransduction
Blood vessels are permanently subjected to mechanical forces in the form of
stretch, encompassing cyclic mechanical strain due to the pulsatile nature of blood flow, and shear stress. Blood pressure is the major determinant of
vessel stretch. It creates radial and tangential forces that counteract the
effects of intraluminal pressure and affect all cell types in the vessel. In
comparison, fluid shear stress results from the friction of blood against
the vessel wall, and it acts in parallel to the vessel surface. Accordingly,
shear is sensed principally by endothelial cells, strategically located at the
interface between the blood and the vessel wall. Alterations in stretch or
shear stress invariably produce transformations in the vessel wall that will aim to accommodate the new conditions and to ultimately restore the basal
levels of tensile stress and shear stress (1,2). Hence, while acute changes
in stretch or shear stress correlate with transient adjustments in vessel dia-
meter, mediated through the release of vasoactive agonists or change
in myogenic tone, chronically altered mechanical forces usually instigate
important adaptive alterations of vessel wall shape and composition.
The concept of vascular remodeling has therefore been used to describe these transformations that occur in vessels undergoing mechanical stresses.